pathology of the blood vessels

1. DISEASES OF THE BLOOD VESSELS
• PRESENTER : DR ALLY RASHID (CUHAS/MMED/6000438/T/20)
• FACILITATOR : DR EDRICK ELIAS MD, MMED PATHOLOGY

2. CONTENT
• ANATOMY OF BLOOD VESSELS
• ARTERIOSCLEROSIS
• ATHEROSCLEROSIS
• VASCULITIS
• ANUERISMS
• COMMON DISEASES OF VEINS

3. The Blood Vessels
• The blood containing oxygen, nutrients and
metabolites is routed through arteries, arterioles,
capillaries, venules and veins.
• These blood vessels differ from each other in their
structure and function.

4. ARTERIES
• 1. Tunica intima This is the inner coat of the artery. It is composed of
the lining endothelium, subendo thelial connective tissue and
bounded externally by internal elastic lamina.
• 2. Tunica media is the middle coat of the arterial wall, bounded
internally by internal elastic lamina and externally by external elastic
lamina. This layer is the thickest and consists mainly of smooth
muscle cells and elastic fibres.
• 3.Tunica adventitia The outer coat of arteries is the tunica adventitia.
It consists of loose mesh of connective tissue and some elastic fibres
that merge with the adjacent tissues. This layer is rich in lymphatics
and autonomic nerve fibres.

5. • There are structural variations in three types of arteries:
• Large, elastic arteries such as the aorta, common carotid, major
pulmonary, and common iliac arteries have very high content of
elastic tissue in the media and thick elastic laminae
Medium-sized, muscular arteries are the branches of elastic
arteries. All the three layers of arterial wall are thinner than in the
elastic arteries. The internal elastic lamina appears as a single wavy
line while the external elastic lamina is less prominent. The media
primarily consists of smooth muscle cells and some elastic fibres

7. MEDIUM SIZE ARTERIES

8. • Arterioles consist of a layer of endothelial cells in the intima, one or
two smooth muscle cells in the media and small amount of collagen
and elastic tissue comprising the adventitia. The elastic laminae are
virtually lost

9. • VEINS
• The walls of the veins are thinner, the three tunicae (intima, media
and adventitia) are less clearly demarcated, elastic tissue is scanty
and not clearly organised into internal and external elastic laminae.
The media contains very small amount of smooth muscle cells with
abundant collagen.
• Capillaries are about the size of an RBC (7-8 µm) and have 1-2
endothelial cells but no media

10. ARTERIOSCLEROSIS
• Arteriosclerosis is a general term used to include all conditions with
thickening and hardening of the arterial walls
• The following morphologic entities are included under
arteriosclerosis:
• I. Senile arteriosclerosis (affects arteries)
• II. Hypertensive arteriolosclerosis (affects arterioles)
• III. Mönckeberg’s arteriosclerosis (Medial calcific sclerosis) (affects
arteries)
• IV. Atherosclerosis (affects arteries)

11. ATHEROSCLEROSIS
• Atherosclerosis is an thickening and hardening of large and medium-
sized muscular arteries, primarily due to involvement of tunica intima
and is characterised by fibrofatty plaques or atheromas.
• Mostly affected are the
1. Aorta, ( aortic aneurysm)
2. Coronaries ( MI)
3. cerebral arterial systems.( Stroke)

13. • Dyslipidaemia
• chronic dyslipidaemia in itself may initiate endothelial injury and
dysfunction by causing increased permeability. In particular,
hypercholesterolaemia with increased serum concentration of LDL
promotes formation of foam cells, while high serum concentration of
HDL has anti-atherogenic effect
• Diabetis mellitus
• The causes of increased severity of atherosclerosis are complex and
numerous which include endothelial dysfunction, increased aggre
gation of platelets, increased LDL and decreased HDL

15. • Hypetension
• It acts probably by mechanical injury to the arterial wall due to
increased blood pressure. Elevation of systolic pressure of over 160
mmHg or a diastolic pressure of over 95 mmHg is associated with five
times higher risk of developing IHD than in people with blood
pressure within normal range (140/90 mmHg or less).
• Smoking
• The increased risk and severity of atherosclerosis in smokers is due to
reduced level of HDL, deranged coagulation system and accumulation
of carbon monoxide in the blood that produces carboxy haemoglobin
and eventually hypoxia in the arterial wall favouring atherosclerosis.

19. • The clinical effects of atherosclerosis depend upon the size and type
of arteries affected. In general, the clinical effects result from the
following:
• 1. Slow luminal narrowing causing ischaemia and atrophy.
• 2. Sudden luminal occlusion causing infarction necrosis.
• 3. Propagation of plaque by formation of thrombi and emboli.
• 4. Formation of aneurysmal dilatation and eventual rupture.

21. Common site for Aneurysm

22. VASCULITIS
• Arteritis, angiitis and vasculitis are the common terms used for
inflammatory involvement of an artery, arterioles, venules and
capillaries.
• It may occur following invasion of the vessel by infectious agents, or
may be induced by non-infectious injuries such as chemical,
mechanical, immuno logic and radiation injury

24. INFECTIOUS ARTERITIS
• Direct invasion of the artery by infectious agents, especially bacteria
and fungi, causes infectious arteritis.
• It may be found in the vicinity of an infected focus like in tuberculosis,
pneumonia, abscesses, etc. or less frequently may arise from
haematogenous spread of infection such as in infective endocarditis,
septicaemia, etc

25. ENDARTERITIS OBLITERANS
• Endarteritis obliterans is not a disease entity but a pathologic
designation used for non-specific inflammatory response of arteries
and arterioles to a variety of irritants.
• It is commonly seen close to the lesions of peptic ulcers of the
stomach and duodenum, tuberculous and chronic abscesses in the
lungs, chronic cutaneous ulcers, chronic meningitis, and in
postpartum and post-menopausal uterine arteries

27. SYPHILITIC ARTERITIS
• Syphilitic or luetic vascular involvement occurs in all stages of syphilis
but is more prominent in the tertiary stage.
• The changes that are found in the syphilitic arteritis are seen within
the arterial tissue (syphilitic endarteritis) and in the periarterial
tissues (syphilitic peri arteritis).
• Manifestations of the disease are particularly prominent at two
sites—the aorta and the cerebral arteries

28. SYPHILITIC AORTITIS
• Syphilitic involvement of the ascending aorta and the aortic arch is
the commonest manifestation of cardiovascular syphilis.
• It occurs in about 80% cases of tertiary syphilis.
• Preferential involvement of the arch of aorta may be due to
involvement of mediastinal lymph nodes in secondary syphilis.
• The lesions diminish in severity in descending thoracic aorta and
disappear completely at the level of the diaphragm.

31. COMPLICATIONS OF SYPHILITIC AORTITIS
• a) Aortic aneurysm may result from damage to the aortic wall
• b) Aortic incompetence results from spread of the syphilitic process
to the aortic valve ring.
• c) Stenosis of coronary ostia is seen in about 20% cases of syphilitic
aortitis and may lead to progressive myocardial fibrosis, angina
pectoris and sudden death

32. NON-INFECTIOUS ARTERITIS
• II. This group consists of most of the important forms of vasculitis,
more often affecting arterioles, venules and capillaries, and hence
also termed as small vessel vasculitis.
• Serum from many of patients with vasculitis of immunologic origin
show the presence of following immunologic features:
• 1. Anti-neutrophil cytoplasmic antibodies (ANCAs)
• Wegener’s granulomatosis, - PAN
• 2. Anti-endothelial cell antibodies (AECAs)
• SLE, Kawasaki disease and Buerger’s disease.

33. POLYARTERITIS NODOSA
• Is a necrotising vasculitis involving small and medium-sized muscular
arteries of multiple organs and tissues.
• More commonly in adult males than females.
• Most commonly affected organs, in descending order of frequency of
involvement, are the kidneys, heart, liver, gastrointestinal tract,
muscle, pancreas, testes, nervous system and skin.
• The condition is believed to result from deposition of immune
complexes and tumour-related antigens

34. • CHARACTARISTICS
• fever,
• malaise,
• weakness,
• weight loss,
• renal manifestations (albuminuria, haematuria and renal failure),
• vascular lesions in the alimentary tract (abdominal pain and melaena),
peripheral neuritis and hyper tension.

37. WEGENER’S GRANULOMATOSIS
• Wegener’s granulomatosis is another form of necrotising vasculitis
characterised by a clinicopathologic triad consisting of the following
symptom
• i) Acute necrotising granulomas of the upper and lower respiratory
tracts involving nose, sinuses and lungs;
• ii) focal necrotising vasculitis, particularly of the lungs and upper
airways;
• iii) focal or diffuse necrotising glomerulonephritis.

40. TAKAYASU’S ARTERITIS (PULSELESS DISEASE)
• This is a form of granulomatous vasculitis affecting chiefly the aorta
and its major branches and hence is also referred to as aortic arch
syndrome. The disease affects chiefly young women and is typically
• CHARACTERISED by
1.absence of pulse in both arms and presence of ocular manifestations.
2.myocardial infarction,
3 .congestive heart failure and
4.neurologic deficits.
The etiology of Takayasu’s arteritis is not known but the autoimmune reaction
to aortic tissue has been suggested as the possible cause

42. KAWASAKI’S DISEASE (mucocutaneous lymph
node syndrome’,)
• It is an acute and subacute illness affecting mainly young children and
infants.
• febrile illness with mucocutaneous symptoms like erosions of oral
mucosa and conjunctiva, skin rash and lymphadenopathy.
• The etiology is unknown; possible causes considered are infectious,
genetic, toxic and immunological.
• The most characteristic finding is the presence of multiple aneurysms
of the coronaries detected by angiography

44. BUERGER’S DISEASE (THROMBOANGIITIS
OBLITERANS)
• Affecting chiefly small and medium-sized arteries and veins of the
extremities and characterised by acute and chronic occlusive
inflammatory involvement.
• The disease affects chiefly men under the age of 35 years who are
heavy cigarette smokers
• CHARACTARISED by claudication due to ischaemia manifested by
intense pain affecting the limbs, more commonly the legs.
• Eventually, gangrene of the affected extremities occurs requiring
amputation

46. RAYNAUD’S DISEASE AND RAYNAUD’S
PHENOMENON
• Raynaud’s disease is not a vasculitis but is a functional vasospastic
disorder affecting chiefly small arteries and arterioles of the
extremities, occurring in otherwise young healthy females.
• The disease affects most commonly the fingers and hands.
• The ischaemic effect is provoked primarily by cold but other stimuli
such as emotions, trauma, hormones and drugs also play a role.
Clinically,
• pallor,
• cyanosis,
• redness,

48. • Raynaud’s phenomenon differs from Raynaud’s disease in having an
underlying cause e.g. secondary to artherosclerosis, connective tissue
diseases like scleroderma and SLE, Buerger’s disease, multiple
myeloma, pulmonary hypertension and ingestion of ergot group of
drugs

49. ANEURYSMS
• An aneurysm is defined as a permanent abnormal dilatation of a
blood vessel occurring due to congenital or acquired weakening or
destruction of the vessel wall.
• Most commonly, aneurysms involve large elastic arteries, especially
the aorta and its major branches.
• Aneurysms can cause various illeffects such as thrombosis and
thromboembolism, alteration in the flow of blood, rupture of the
vessel and compression of neighbouring structures.

50. CLASSIFICATION OF ANEURYSMS
• A. Depending upon the composition of the wall
• 1 True aneurysm composed of all the layers of a normal vessel wall.
• 2. False aneurysm having fibrous wall and occurring often from
trauma to the vessel.

51. • B. Depending upon the shape
• 1. Saccular having large spherical outpouching.
• 2. Fusiform having slow spindle-shaped dilatation.
• 3. Cylindrical with a continuous parallel dilatation.
• 4. Serpentine or varicose which has tortuous dilatation of the vessel.
• 5. Racemose or circoid having mass of inter communicating small
arteries and veins

53. • Based on pathogenetic mechanisms
• 1. Atherosclerotic (arteriosclerotic) aneurysms
• 2. Syphilitic (luetic) aneurysms.
• 3. Dissecting aneurysms (Dissecting haematoma).
• 4. Mycotic aneurysms.
• 5. Berry aneurysms
• The three common types of aortic aneurysms—atherosclerotic,
syphilitic and dissecting,

55. The clinical effects of atherosclerotic
aneurysms
• 1. Rupture of the atherosclerotic aneurysm is the most serious and
fatal complication. The risk of rupture depends upon the size and
duration of the aneurysm and the blood pressure.
• Rupture of abdominal aneurysm may occur either into the
peritoneum or into the retroperitoneum resulting in sudden and
massive bleeding.
• A ruptured aneurysm is more likely to get infected.

56. • 2.Compression
• The atherosclerotic aneurysm may press upon some adjacent
structures such as compression of ureter and erosion on the vertebral
bodies.

57. • 3. Arterial occlusion
• Atherosclerotic aneurysms of the abdominal aorta may occlude the
inferior mesenteric artery, or there may be development of occlusive
thrombosis.
• However, collateral circulation develops slowly and is nearly always
sufficient so as not to produce effects of ischaemia.
Thromboembolism is rather common in abdominal aneurysms

58. The clinical manifestations in syphilitic
aneurysms
• 1. Rupture Syphilitic aneurysm is likely to rupture causing massive
and fatal haemorrhage into the pleural cavity, pericardial sac, trachea
and oesophagus.
• 2. Compression The aneurysm may press on the adjacent tissues and
cause symptoms such as on trachea causing dyspnoea, on
oesophagus causing dysphagia, on recurrent laryngeal nerve leading
to hoarseness; and erosion of vertebrae, sternum and ribs due to
persistent pressure.

59. • . 3. Cardiac dysfunction
• When the aortic root and valve are involved, syphilitic aneurysm
produces aortic incompetence and cardiac failure. Narrowing of the
coronary ostia may further aggravate cardiac disease.

60. CHEST X RAY SHOWING ANEURYSM

61. DISSECTING ANEURYSMS
• The term dissecting aneurysm is applied for a dissecting haematoma
in which the blood enters the separated (dissected) wall of the vessel
and spreads for varying distance longitudinally.
• The most common site is the aorta and is an acute catastrophic aortic
disease.
• The condition occurs most commonly in men in the age range of 50 to
70 years. In women, dissecting aneurysms may occur during
pregnancy.

62. PATHOGENESIS
• i) Hypertensive state
• About 90% cases of dissecting aneurysm have hypertension which
predisposes such patients to degeneration of the media
• ii) Non-hypertensive cases
• a) Marfan’s syndrome,
• b)Development of cystic medial necrosis of Erdheim, especially in old age.
• c) Iatrogenic trauma during cardiac catheterisation or coronary bypass
surgery.
• d) Pregnancy, for some unknown reasons.

66. COMMON DISEASES OF VEINS
• VARICOSITIES
• Are abnormally dilated and tortuous veins. The veins of lower
extremities are involved most frequently, called varicose veins.
• The veins of other parts of the body which are affected are the lower
oesophagus (oesophageal varices), the anal region (haemorrhoids)
and the spermatic cord (varicocele)

67. Varicose Veins
• Varicose veins are permanently dilated and tortuous superficial veins
of the lower extremities, especially the long saphenous vein and its
tributaries.
• Adult females are affected more commonly than the males, especially
during pregnancy.
• This is attributed to venous stasis in the lower legs because of
compression on the iliac veins by pregnant uterus.

68. ETIOPATHOGENESIS
• i) Familial weakness of vein walls and valves is the most common
cause.
• ii) Increased intraluminal pressure due to prolonged upright posture
e.g. in nurses, policemen, surgeons etc.
• iii) Compression of iliac veins e.g. during pregnancy, intravascular
thrombosis, growing tumour etc.
• iv) Hormonal effects on smooth muscle.
• v) Obesity.
• vi) Chronic constipation.

69. EFFECTS OF VARICOSE VEINS OF THE LEGS
• Venous stasis which is followed by
• congestion,
• oedema,
• thrombosis,
• stasis,
• dermatitis,
• cellulitis and ulceration.
• Secondary infection results in chronic varicose ulcers

70. PHLEBOTHROMBOSIS AND
THROMBOPHLEBITIS
• The most common locations for phlebothrombosis and
thrombophlebitis are the deep veins of legs accounting for 90% of
cases; it is commonly termed as deep vein thrombosis (DVT)

71. ETIOPATHOGENESIS
• Venous thrombosis that precedes thrombophlebitis is initiated by
triad of changes:
• endothelial damage,
• alteration in the composition of blood and
• venous stasis.
• The factors that predispose to these changes are cardiac failure, malig
nancy, use of oestro gen-containing compounds, postoperative state
and immobility due to various reasons

72. Special Types of Phlebothrombosis
• 1. THROMBOPHLEBITIS MIGRANS
• 2. PHLEGMASIA ALBA DOLENS
• 3. PHLEGMASIA CERULEA DOLENS
• 4. SUPERIOR VENA CAVAL SYNDROME
• 5. INFERIOR VENA CAVAL SYNDROME